Monocyte chemotactic protein induced protein 1 (MCPIP1) fails to affect adipogenesis in immortalized mouse embryonic fibroblasts (iMEF) (LB149)

Abstract

Background: Increased adipogenesis is associated with chronic inflammation. MCPIP1 has been shown to suppress inflammation through regulating pro‐inflammatory cytokines in the immune system. Recent studies found that MCPIP1 is involved in the process of adipogenesis in 3T3‐L1 cells but the results are controversial. Our preliminary data indicates that MCPIP1 knockout impaired hepatic insulin signaling. The current study was designed to deterimine if MCPIP1 affects adipogenesis by regulating the insulin signal transduction pathway. Methods: MEFs were isolated from both MCPIP1 heterozygous (no phenotypic changes) and knockout C57/BL6 mice and immortalized. At 2 days post‐confluency, the cells were treated with or without a differentiation cocktail containing dexamethasone, IBMX, trogliterazone, and different concentrations of insulin. After 48 hours, cells were switched to medium containing 10% FBS with or without the different concentrations of insulin for the remainder of the differentiation period. Adipocyte differentiation was measured using Oil Red‐O staining by visualizing the intracellular lipid droplets. Lipids were extracted with isopropanol. The concentration of lipid was measured, calculated, and expressed by normalizing to the protein concentration. Results: Although a slight increase in adipogenesis was seen in the MCPIP1 KO model compared to the heterozygous model, overall there was no significant difference between these groups (p>0.05). Also, no difference in adipogenesis was observed among the different concentrations of insulin groups in cells from either heterozygous or MCPIP1 KO mice (p>0.05). Conclusion: From the data we collected thus far, we conclude that MCPIP1 might not play a key role in adipogenesis in iMEFs. Insulin may not be required to stimulate adipogenesis in iMEFs isolated from MCPIP1 knockout and heterozygous mice.Grant Funding Source: Supported by ATSU‐KCOM Biomedical Sciences Program